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Why blood pressure changes in long-lasting pain

THURSDAY6 OCTOBER 201611:24 AM

A new study from NeuRA has uncovered the underlying brain mechanisms that cause some people to experience an increase in blood pressure after being exposed to long-lasting pain, while others experience a decrease in blood pressure.

The team at NeuRA have developed a world-first technique that allows them to measure muscle sympathetic nerve activity (MSNA), which is a determinant of blood pressure, while using functional magnetic resonance imaging (fMRI) to see which areas of the brain are involved in causing the change in blood pressure.

An increase in MSNA results in an increase in blood pressure, while a decrease in MSNA results in a decrease in blood pressure.

For this study, fine microelectrodes were inserted into the side of the knee where spontaneous bursts of MSNA were measured. At the same time, fMRI images identified which areas of the brain lit up in a similar fashion.

“If you think of the bursts of nerve activity as being similar to flashes from a lighthouse, we were able to see which areas of the brain responded in a similar fashion or at a similar rate,” says Prof Vaughan Macefield.

The study revealed several core areas of the brain that were strongly coupled with MSNA bursts. The prefrontal and cingulate cortices, precuneus, nucleus accumbens, caudate nucleus and dorsomedial hypothalamus areas increased in activity in those who experienced an increase MSNA, or remained at baseline or decreased in people whose MSNA decreased.

These areas are involved in higher-order emotional and cognitive functions, researchers said. However, pain catastrophising, pain vigilance and anxiety levels were not predictors of change in blood pressure. In addition, there was no difference in pain parameters such as the intensity, speed or descriptors.

These results suggest that the differing responses in blood pressure due to muscle pain result from the activation of a neural pathway thought to be responsible for cardiovascular responses to psychological rather than physiological stressors. However, researchers warn this may not fully explain why some people with chronic pain go on to develop hypertension.

“Although there is a well-documented relationship between psychological variables such as pain catastrophising and the development of chronic pain, our findings suggest that these variables do not predict the MSNA response to pain and likely do not play a role in hypertension involved in chronic pain,” said Prof Macefield.

“Many people who experience chronic pain often go on to develop hypertension, but we haven’t yet been able to use physiological or psychological factors to predict who is likely to do so. Understanding the underlying neural cause of these differential responses to pain opens up a whole new avenue of research to explore.”

37 participants lay on an MRI bed with a microelectrode placed in their leg to measure MSNA bursts.

Prior to the scanning period, five minutes of continuous blood pressure was recorded. Heart rate was monitored throughout the scanning via a pulse transducer placed on the big toe.

During the fMRI scan a hypertonic saline solution was inserted into the calf muscle. Each subject was unaware when the saline infusion was to begin and was constantly adjusted to maintain a pain level of five out of 10.

At the completion of the scanning session, each subject was asked to draw the area of perceived pain on a standard diagram of the leg.